Christian Marinaccio, PhD Candidate, of Northwestern University, describes research he is conducting in the laboratory of John D. Crispino, PhD, which shows the loss of the tumor suppressor gene LKB1/STK11 facilitates progression of myeloproliferative neoplasms to acute myeloid leukemia (Abstract 1).
Ari M. Melnick, MD, of Weill Cornell Medicine, discusses the BCL10 mutation in patients with activated B-cell–like diffuse large B-cell lymphoma, and his study results which showed that the mutation should be considered as a biomarker for ibrutinib resistance so that alternative targeted treatments can be prioritized (Abstract 3).
Matthew S. Davids, MD, of Dana-Farber Cancer Institute, summarizes three key studies from a session he co-moderated on ibrutinib plus venetoclax for first-line treatment of patients with chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL), long-term responses to these agents for relapsed and refractory CLL, and undetectable minimal residual disease following fixed-duration treatment with venetoclax and rituximab for CLL (Abstracts 123, 124, and 125).
Steven M. Horwitz, MD, of Memorial Sloan Kettering Cancer Center, discusses phase II data from the Primo trial, which support continued evaluation of duvelisib as a treatment option for relapsed or refractory peripheral T-cell lymphoma due to consistent response rates (Abstract 44).
Lena E. Winestone, MD, MSHP, of the University of California, San Francisco and Benioff Children’s Hospital, reviews different aspects of bias in treatment delivery, including patient selection for clinical trials; racial and ethnic disparities in survival for indolent non-Hodgkin diffuse large B-cell lymphomas; and end-of-life hospitalization of patients with multiple myeloma, as well as outcome disparities (Abstracts 207-212).
Farhad Ravandi, MD, of The University of Texas MD Anderson Cancer Center, offers his expert perspective on key treatment studies in acute myeloid leukemia on the use of gilteritinib, consolidation chemotherapy, venetoclax, cladribine, azacitidine, quizartinib, decitabine, and CPX-351 (Session 616 [Abstracts 24- 29]).
